- Immune System in COVID19- Blessing or Curse?
- Reference: https://www.nature.com/articles/s41587-020-0602-4
- The novel coronavirus SARS-CoV-2 infection is characterized by a highly variable course. Some of the infected patients are asymptomatic in contrast to several others who find their way to ICU. After studying the nasopharyngeal and bronchia at the single-cell resolution, our lab has discovered that the immune system acts like a “double-edged sword” in the progression of the disease. Here, we have shown that the epithelial cells affected by the virus trigger a “distress call” to the immune system that attracts the immune cells to the site of infection to combat the virus. However, the migrating immune cells occasionally cross their limit and, due to excessive reaction, sometimes cause high inflammation leading to more significant damage than the virus itself. Interestingly, the signaling protein interferon, also known as our central defense strategy against viral infections contribute to the epithelial cells producing more ACE2 and hence become more vulnerable to viral infection. The key transcriptomic differences in the critical patients as compared to the moderate ones including more robust communication between the epithelial and immune cell types & presence of inflammatory macrophages likely contribute to clinical observations of heightened inflammatory tissue damage, lung injury, and respiratory failure. From our data, we suggest that pharmacologic inhibition of the CCR1 and/or CCR5 pathways might suppress the immune hyperactivation in critical COVID-19.
- Summary by: Olivia Debnath, Digital Health Centre, Berlin Institute of Health, Charité – Universitätsmedizin Berlin, Germany
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